The Amygdala: Corticotropin-Releasing Factor, Steroids, and Stress
Abstract
The possible function of corticotropin-releasing factor (CRF), adrenal steroids, and gonadal steroids in amygdala-mediated responses to anxiogenic or stressful stimuli is reviewed. The amygdala is part of an endogenous CRF circuitry within the brain that mediates neuroendocrine, autonomic, and behavioral changes in response to stress. The amygdala contains CRF-expressing neurons that communicate with widespread regions of the neural axis. High densities of CRF, CRF-binding protein, and CRF receptors are located in the amygdala. Direct injections of CRF into the amygdala produce anxiety-like behaviors. Release of endogenous CRF can be measured in the amygdala during stress. Potent anxiolytic actions are observed when CRF receptor antagonists are administered into the amygdala. CRF-containing neurons of the amygdala can be directly modulated by alterations in circulating glucocorticoids through glucocorticoid receptors, which are expressed in amygdaloid CRF-containing neurons. Gonadal steroid hormone receptors are found in the amygdala. They are not located in CRF immunoreactive neurons, but they are located adjacent to CRF-expressing neurons and in amygdaloid neurons that are likely to participate in central autonomic and neuroendocrine circuitry. Differences are noted between the steroid influences in the amygdala of male and female animals. Also, evidence is reviewed suggesting a modulatory role in the amygdala for gonadal and adrenal steroids in behavioral, autonomic, and neuroendocrine responses to anxiogenic stimuli.
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The central amygdala nucleus (CEA) is rich in stress hormones and their receptors and contributes to processing of stress signals.
“The CEA is rich in stress hormones and their receptors,98, 99, 100, 101 and contributes to processing of stress signals.102, 103, 104”
From Preferential loss of dorsal-hippocampus synapses underlies memory impairments provoked by short, multimodal stress (2014) · cites this paper as [99]
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- Authors
- Gray, T. S., & Bingaman, E. W.
- Affiliations
- Loyola University Medical Center (US)
- Venue
- Critical Reviews™ in Neurobiology
- Publisher
- Begell House
- Published
- 1996
- Volume
- 10
- Issue
- 2
- Pages
- 155-168
- ISSN
- 0892-0915 (ISSN-L)
- OpenAlex
- W2008776698
- Cited by
- 230
- References
- 0
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- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Critical Reviews in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns020041-09)
- National Institute of Neurological Disorders and Stroke (R01 NS20041)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- amygdala, corticotropin-releasing factor, glucocorticoids, adrenal steroids, sex steroids, stress response, anxiety, CRF receptors, CRF-binding protein, glucocorticoid receptor, sex differences, autonomic responses
- MeSH terms
- Amygdala, Animals, Corticotropin-Releasing Hormone, Humans, Gonadal Steroid Hormones, Stress, Physiological
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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